Endocrine System II (b) Flashcards

1
Q

Celluar Components of the Adeno-Hypophysis (Anterior pituitary)

A

basophilic, eosinophilic and
chromophobic cytoplasm

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2
Q

Anterior Pituitary (Adeno-Hypophysis) produces?

A

PRL, GH,
ACTH, FSH, LH and TSH

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3
Q

Celluar Components of the Posterior Pituitary (Neuro-Hypophysis)

A

modified glial cells (pituicytes) and axonal
processes from Hypothalamus

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4
Q

Posterior Pituitary (Neuro-Hypophysis) produces?

A

Oxytocin and ADH (or Vasopressin)

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5
Q

loc of the pituitary gland

A

Base of the brain, within Sella turcica
(bellow the hypotahlamus connected by a stalk-composed of axons)

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6
Q

Cause of Hyperpituitarism

*Excessive secretion of trophic hormones

A

Anterior Pituitary Aden.

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7
Q

Cause of Hypopituitarism

* Deficiency of trophic hormones

A

Ischaemic injury, surgery, radiation, inflammatory reactions, Non-functional Pituitary Adenomas (through compression of adjacent normal tissue)

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8
Q

Complictions of Pituitary Adenoma

A

i. Visual field defects (bitemporal hemianopsia),
ii. Elevated intra-cranial pressure (headache, nausea, vomiting),
iii. Seizures or obstructive hydrocephalus
iv. Pituitary apoplexy (acute haemorrhage in an Adenoma)

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9
Q

Causes of Hyperpituitarism
& Pituitary Adenomas

A
  • Anterior Pituitary Adenoma (most common)
  • Hyperplasia
  • Pituitary Carcinoma
  • Secretion of hormones by extra-pituitary tumour
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10
Q

patho of Hyperpituitarism
& Pituitary Adenomas

A

*GNASI gene mutations (a-subunit of Gs protein)
–> Persistent generation of cAMP –> Unchecked cellular proliferation;
About 40% of GH-secreting Somatotroph Cell Adenomas

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11
Q

Genes involved in the development of familial Pituitary Adenomas (Prolactinoma)?

A

MEN 1, CDKNIB, PRKARIA
and AIP

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12
Q

* Familial Pituitary Adenomas

Mutations of ——– gene are associated with an
aggressive behaviour , such as invasion and
recurrence

A

TP53

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13
Q

Microscopic Findings:
* Uniform, polygonal cells arranged in sheets, cords or papillae
* Uniform or pleomorphic nuclei (Monomorphic
appearance of tumour cells)
* Low mitotic index
* Acidophilic, basophilic or chromophobic cytoplasm
* Sparse supporting connective tissue or reticulin
* Small round cells
* Small round nuclei
* Pink to blue cytoplasm

A

PITUITARY ADENOMAS (Anterior)

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14
Q

Epi of Prolactinomas

A

Most common type of functional
Pituitary Adenomas

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15
Q

CF of Prolactinomas

A
  • Hyperprolactinaemia
  • Amenorrhoea
  • Galactorrhoea
  • Loss of libido
  • Infertility
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16
Q

What is Pituitary Stalk effect ?

A

Hyperprolactinaemia caused by a mass
(other than Prolactinoma
) in the supra-sellar
compartment –> which inhibits the normal inhibitory influence of Hypothalamus on Prolactin secretion

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17
Q

Microscopic features:
* Chromophobic cells (clear cells)
* Sphaerical microcalcifications

A

Prolactinomas

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18
Q

Epi of Growth Hormone-Producing
(Somatotroph) Adenomas

A

Second most common type of
functional Pituitary Adenomas

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19
Q

Microscopic features:
* Densely or sparsely granulated cells
* Paranuclear “fibrous body”

A

Growth Hormone-Producing (Somatotroph) Adenomas

*Paranuclear bodies = indication of Pituitary adenomas

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20
Q

* GH-Producing (Somatotroph) Adenomas

Overproduction and release of GH leads to hepatic
secretion of —— –>
–> In cases of prepubertal children (before closure of epiphyses) —-> —————–
–> After closure of epiphyses –> ————–

A

secretion of IGF-1
Before –> Giganitism
After (adults) –> Acromegaly

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21
Q

CF of Growth Hormone-Producing
(Somatotroph) Adenomas

A
  • Gigantism or Acromegaly
  • Abnormal Glucose tolerance
  • Diabetes Mellitus
  • Generalised muscle weakness
  • Hypertension
  • Arthritis
  • Osteoporosis
  • Congestive Heart Failure
22
Q

Epi of ACTH-Producing Adenomas

A
  • Commonly, Micro-Adenomas
  • Clinically silent or manifested as Cushing Syndrome
23
Q

Cause of Nelson Syndrome

A

Development of large (Macro-adenomas), aggressive ACTH Adenomas, after removal of both Adrenal Glands,
for treatment of Cushing Syndrome

24
Q

Absence of Adrenal Glands –> {No/yes} Hypercortisolism

A

No

25
Q

CF of Nelson Syndrome

A

i. Hyperpigmentation of the skin,
ii. Headaches and
iii. Vision impairment

26
Q

Lab findings of Nelson Syndrome

A

levels of ACTH and
β-MSH

27
Q

CF of Gonadotroph (FSH- and LH-producing) Adenomas

A
  • Impaired vision,
  • headaches,
  • diplopia (double vision),
  • pituitary apoplexy
28
Q

Immunohistochemistry of Gonadotroph (FSH- and LH-producing) Adenomas

A

+ve for : common Gonadotropin α-subunit , the specific β-FSH and β-LH subunits

29
Q

Epi of Thyrotroph (TSH-producing) Adenomas

A
  • 1% of Anterior Pituitary Adenomas
  • Rare cause of Hyperthyroidism
30
Q

Epi of Non-functional Pituitary Adenomas

A

25% of all pituitary tumours (posterior)

31
Q

CF of Non-functional Pituitary Adenomas

A
  • Typical presentation of mass effects
  • Compromise of the residual Anterior
    Pituitary –> Hypopituitarism
32
Q

Epi of Pituitary Carcinomas

A

Rare occurrence

33
Q

Microscopic features:
Rosettes of small cells
Monomorphic (pleomorphic) chromatin-rich nuclei

A

Null-Cell Adenomas (aka Hormone-negative adenomas)

*Null-cell adenomas have abscense of immuno-histochemical reactivity

34
Q

———— : Hypofunction of the Anterior Pituitary, after loss or absence of >75% of the Anterior Pituitary
parenchyma

A

Hypopituitarism

35
Q

Causes of Hypopituitarism

A

1) Hypopituitarism, accompanied by Diabetes
Insipidus
, is almost always of hypothalamic
origin
2) Non-functioning Pituitary Adenomas
3) Ablation of the Pituitary Gland by surgery or irradiation
4) Inflammatory disorders (e.g. Sarcoidosis, Tbc),
5) trauma and metastatic neoplasms
6) Sheehan’s syndroms or postpartum necrosis of Anterior Pituitary Gland
7) Other causes of ischaemic necrosis: DIC, sickle cell anaemia, trauma, shock, etc.

36
Q

CF of Hypopituitarism (depending on hormone(s) lacking)

  • GH-deficiency –> —–
  • GnRH deficiency –> ——- (F); —— (M)
  • PRL deficiency –> ———-
  • TSH deficiency –> ——–
  • ACTH deficiency –> ———
A
  • GH-deficiency –> Dwarfism (in children)
  • GnRH deficiency–> Amenorrhoea and Infertility
    (F); Decreased Libido and Impotence (M)
  • PRL deficiency –> Failure of postpartum Lactation
  • TSH deficiency –> Hypo-Thyroidism
  • ACTH deficiency –> Hypo-Adrenalism

*GnRH: Gonadotropin-Releasing Hormone

37
Q

causes of Empty sella Turcica

A
  • Pituitary compression through herniation of the Arachnoidea (Arachnoid mater)
  • Sheehan syndrome
  • Total infarction of an Adenoma
  • Operation or Radiation of the Hypophysis
38
Q

Posterior Pituitary Syndromes examples

A

1) Central Diabetes Insipidus
2) Syndrome of Inappropriate ADH (SIADH) secretion

39
Q

* Posterior Pituitary Syndromes

Causes of Syndrome of Inappropriate ADH (SIADH) secretion

A
  • Ectopic ADH secretion, by a malignant neoplasm
    (e.g. SCLC)
  • Non-neoplastic diseases of the lung
  • Local injury to the Hypothalamus or Neuro-Hypophysis
40
Q

* Posterior Pituitary Syndromes

patho of Syndrome of Inappropriate ADH (SIADH) secretion

A

Resorption (loss) of excessive amounts of free water –> Hyponatraemia (low Na+)

41
Q

* Posterior Pituitary Syndromes

CF of Syndrome of Inappropriate ADH (SIADH) secretion

A
  • Cerebral oedema –> Neurologic dysfunction
  • Normal blood volume and NO peripheral oedema
42
Q

* Posterior Pituitary Syndromes

Cause of Central Diabetes Insipidus

A
  • Idiopathic
  • Head trauma
  • Neoplasms
  • Inflammatory disorders
43
Q

* Posterior Pituitary Syndromes

Lab findings of Central Diabetes Insipidus

A

Increased serum Sodium and osmolality, as a result of excessive renal loss of free H2O

44
Q

* Posterior Pituitary Syndromes

Cf of Central Diabetes Insipidus

A
  • Polyuria (dilute urine, with low specific gravity)
  • Polydipsia
45
Q

MoI of MEN-1 + mutation

A

MoI: AD
Mutation: inactivation of both alleles of the MEN-1 gene

46
Q

MEN-1 loc+ examples

A
  • 1) parathyroid –> Primary Hyperparathyroidism, due to Hyperplasia or Adenoma; Most common
    manifestation in MEN-1 (80-95% of cases)
    2) Pituitary –> Prolactinoma (Prolactin-secreting Macroadenoma)
    3) Pancrease –> *insulinomas** (zollinger Elison syndrome)
47
Q

MEN-2 moI+MUTATION

A

MoI: AD
Mutation: germ-line RET mutations, activating mutations of the RET proto-oncogene

48
Q

MEN-2

All persons with germ-line RET mutations should
undergo prophylactic thyroidectomy to prevent the unavoidable development of ?

A

Medullary
Carcinomas

49
Q

Loc of MEN-2A +examples

A

1) Thyroid: Medullary Carcinomas
2) Adrenal Medulla –> Pheochromocytomas;
3) Parathyroid: 10-20% of patients –>
Development of Parathyroid Gland Hyperplasia
–> Primary Hyperparathyroidism

50
Q

Endocrine Manifestations in MEN-1

A
  • Zollinger-Ellison Syndrome associated with
    Gastrinomas
  • Hypoglycaemia associated with Insulinomas
51
Q

MEN-2B involves?

A

Thyroid (Medullary carcinoma) and the Adrenal Medulla (pheochromocytoma)

Thyroid and Adrenal Medulla disease shows
similarities to MEN-2A, with the following
differences:
* MEN-2B patients do not develop Primary
Hyperparathyroidism

* Extra-endocrine manifestations in MEN-2B
patients:
* Ganglio-Neuromas of mucosal sites
(GI tract, lips, tongue)

* Marfanoid habitus